Introduction and aim: An accidental or intentional paracetamol overdosage is a common condition, with hepatic injury as a common complication. Kidney could be injured in association with hepatic injury. Prevention and/or proper treatment is markedly important. The current study aimed to investigate the role of vitamin D (VD) in acute paracetamol-induced hepatorenal damage. Methodology: Fourty male Wister rats were divided into 4 equal groups. The negative control (NC), the positive control (PC) (received paracetamol 1200mg/kg), prophylactic group (received VD (1000 IU/Kg/day) before induction of toxicity and treatment continued after induction); and the treatment group with VD (2000 IU/Kg/day) for five successive days after induction of toxicity, for three successive cycles. VD levels, serum liver enzymes, total protein, albumin, serum urea and creatinine were estimated. The concentrations of interferon-γ (IFN- γ), interleukins (IL1β, IL4, IL10, and IL-17) in the tissue lysate were determined. The oxidative stress indicators and antioxidant enzymes (glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), glutathione (GSH) and Malonaldehyde (MDA)) were also measured. Results: Liver enzymes, serum urea and creatinine were increased in PC than NC groups, and were significantly reduced in prophylactic and treatment groups. But not return normal values, and prophylactic group is better. Total proteins and albumin significantly reduced by paracetamol toxicity and returned to near normal with VD supplementation. Vitamin-D levels were significantly reduced in PC than NC groups. However, it was significantly increased in prophylactic and treatment groups than NC and PC groups. IFN- γ, IL-1β, IL-17, and MDA were significantly increased, while IL-10, GPx, CAT, and GSH were significantly reduced in PC than NC groups. Prophylactic and treatment groups improved the values. However, SOD significantly reduced in PC than NC group. Vitamin D was significantly and inversely correlated with ALT, AST, ALP, albumin, creatinine, liver and kidney IFN-γ, IL-1β, IL-17 and MDA. But, it was proportionately and significantly correlated with liver and kidney IL-10. Conclusion: Acute paracetamol toxicity alters hepatic and renal VD homeostasis through oxidative stress and pro-inflammation. Vitamin D supplementation had an ameliorative action on hepatorenal injury, and the long duration of VD supplementation had better outcome.
Objective: Cigarette smoking harms all body systems, and its effects are primarily related to nicotine. However, the heavy metal content (mainly lead and cadmium) could add to nicotine's hazardous effects. Thus, the current study aimed to investigate the effect of cigarette smoking content of cadmium and lead on bone mineral density. Subjects and Methods: A retrospective analysis of data from active, passive, and non-smokers (every 70 subjects) was analyzed for patient demographics, laboratory investigation, serum cotinine (as a confirmatory marker of smoking, bone mineral density (BMD), blood and urinary levels of cadmium and lead). Results: Hemoglobin concentrations and red blood cell count were significantly reduced, while erythrocyte sedimentation rate and liver enzymes were significantly increased in active and passive smokers than non-smokers. Serum cadmium, lead, and cotinine were raised considerably in passive and active than non-smokers (0.47±0.05, 21.94±3.99, 5.35±0.90 in active, 0.32±0.09, 18.91±3.30, and 4.35±0.89 in passive, versus 0.09±0.06, 9.84±2.63, and 1.28±0.21 in the control group, successively). Bone mineral density was reduced in active and passive than non-smokers at the radial shaft, femoral neck, and spine. Cotinine was significantly and proportionately correlated with serum cadmium and lead and inversely correlated with bone mineral density. Furthermore, cadmium and lead were inversely correlated with BMD. Conclusion: Cigarettesmoke was associated with higher concentrations of cadmium, and lead may directly and indirectly share in the harmful effects of smoking on BMD. Keywords: Bone Mineral Density, Cotinine, Toxic Heavy Metals, Smoking
Article informationBackground: Cannabis is a versatile plant in conventional medicine, and intera-peritoneal infusion of its hydroalcoholic extract reduced sperm motility substantially over time. Seminiferous tubule diameter and sperm count both significantly reduced when as opposed to the control group. The reproductive system of animals undergoes morphological and physiological alterations as a result of chronic ethanol intake.Vitamin C has a crucial part in the male reproductive system and plays an antioxidant role in organisms by scavenging reactive oxygen species [ROS] created by oxidizing agents. Aim of the work:Evaluation of effects of ethanol and cannabis consumption on adult albinos' reproductive hormones together with histopathological changes. Patients and Methods:The forty animals were divided into four groups: group I, which received only normal saline; group II, which was given oral ethanol [30% [v/v]] at a dose of 2 g/kg; group III, which obtained oral cannabis at an amount of 1.5 mg/kg; and group IV, which acquired ethanol and cannabis by way of ingestion and at the dose indicated above for 28 days. 24 hours after the last dose had been administered, rats were killed, blood was taken, and the resulting serum chemical profile was evaluated. Testes were gathered and measured. Glutathione, catalase, superoxide dismutase peroxidase inhibitor glutathione, malondialdehyde, and histology [hematoxylin and eosin] levels in the testis were measured. Results:In comparison to controls, all experimental groups had significantly lower testosterone levels and testicular glutathione, catalase, superoxide dismutase [SOD], and peroxidase glutathione levels. Malondialdehyde, on the other hand, was markedly elevated in each group of experiments as compared to controls. Alcohol and/or cannabis produced structural abnormalities in the testicles. Conclusion:Ethanol and cannabis abuse had comparable, additive, and synergistic effects that were detrimental to male reproductive health. These effects may be related to how they damaged the body's antioxidant protection mechanism
Background: Background: Acrylamide [ACR] is an essential chemical that is extensively used in many industries and also in laboratories such as treatment of drinking water, wastewater, and soil, production of paper, petroleum, mine, asphalt, dyes, adhesives, and polishes; it is known as a possible carcinogenic compound. Ginger oleoresin's hepatoprotective role can be attributed to its free radical scavenging, anti-inflammatory, and hypolipidemic activities and is partially mediated by the 6-gingerol, shogaol, and zingerone of its active component. Cinnamomum zeylanicum is used to treat many diseases and to prevent such diseases. Aim of the work:Evaluation of the effects of cinnamon and ginger extracts administration on Hepatotoxicity adult male albino rats. Materials and Methods:The groups were divided into five adult male albino rats of a local strain: Group I: acted as a control group with regular salines, group II: hepatotoxicity caused by acrylamid, groups III: hepatotoxicity plus cinnamon, group IV: hepatotoxicity plus ginger, group V: hepatotoxicity plus cinnamon and ginger. Samples for alanine aminotransferase [ALT], aspartate transfers of amino [AST], urea, creatinine, blood urea nitrogen (BUN), total cholesterol, triglyceride [TG], malondialdehyde, tumor necrosis factor α [TNF], superoxide dismutase [SOD], glutathione peroxidase [GPX], as well as total antioxidant [TAC] levels were obtained at the end of the experimental period.Results: Administration of cinnamon and ginger to hepatotoxic rats led to a significant decrease in the mean value of ALT, AST, urea, creatinine, BUN, MDA, and TNF. In addition, it is associated with a significant increase of SOD, GPX, and TAC. Conclusion:Cinnamon and ginger have a protective effect against abnormalities in hepatotoxic rats due to its several protective properties.
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